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At least 991 records · Page 55Linked to original sources
PubMed1996

Acetylcholinesterase and nicotinic acetylcholine receptor expression diverge in muscular dysgenic mice lacking the L-type calcium channel.

L-type Ca2+ channels play critical roles in achieving stabilization of acetylcholinesterase (AChe) mRNA during myogenesis in C2-C12 skeletal muscle cells. To ascertain the importance of this signaling pathway in AChE expression during skeletal muscle development in the animal, we examined AChE mRNA levels in skeletal muscle and heart from control (+/+) and muscular dysgenic (mdg/mdg) mice that lack the skeletal, but not the cardiac, muscle L-type Ca2+ channels. RNase protection analysis showed 40-60% reductions in content of AChE mRNA in leg muscle, but not heart, from newborn and day 18 embryonic dysgenic mice. AChE activity was also reduced uniquely in skeletal muscle. In contrast to AChE transcripts, mRNA levels of the alpha-subunit of the nicotinic acetylcholine receptors (nAChRs) were increased in dysgenic skeletal muscle. Similar alterations in activity and mRNA levels of AChE were also observed form skeletal muscle cell lines derived from mdg mice. Because run-on transcription revealed no corresponding decrease in transcription rate, the decrease in mRNA content is likely a consequence of the inability of the dysgenic muscle cells to stabilize AChE mRNA during differentiation. These findings indicate that L-type Ca2+ channels play an important role in regulation of AChE expression during skeletal muscle development in vivo. The differential influence of muscle dysgenesis on mRNA levels of AChE and nAChRs provides additional evidence for distinct mechanisms of regulation of these two proteins.

Acetylcholinesterase↗
PubMed2001

Interrelations of myogenic response, progressive atrophy of muscle fibers, and cell death in denervated skeletal muscle.

Little is known concerning the time-course and structural dynamics of reactivation of compensatory myogenesis in denervated muscle, its initiating cellular mechanisms, and the relationship between this process and the progression of postdenervation atrophy. The purpose of this study was to investigate the interrelations between temporal and spatial patterns of the myogenic response in denervated muscle and progressive atrophy of muscle fibers. Another objective was to study whether reactivation of myogenesis correlates with destabilization of the differentiated state and death of denervated muscle cells. It has remained unclear whether muscle fiber atrophy was the primary factor activating the myogenic response, what levels of cellular atrophy were associated with its activation, and whether the initiation and intensity of myogenesis depended on the local and individual heterogeneity of atrophic changes among fibers. For this reason, our objective was also to identify the levels of atrophic and degenerative changes in denervated muscle fibers that are correlated with activation of the myogenic response. We found that the reactivation of myogenesis in the tibialis anterior and extensor digitorum longus muscles of the rat starts between days 10-21 following nerve transection, before atrophy has attained advanced level, long before dead cells are found in the tissue. Formation of new muscle fibers reaches its maximum between 2 and 4 months following denervation and gradually decreases with progressive postdenervation atrophy. The myogenic response is biphasic and includes two distinct processes. The first process resembles the formation of secondary and tertiary generations of myotubes during normal muscle development and dominates during the first 2 months of denervation. During this period, activated satellite cells form new myotubes on live differentiated muscle fibers. Most of the daughter myotubes in 1- and 2-month denervated muscle develop on the surface of fast type parent muscle fibers, and some of the newly formed muscle fibers express slow myosin. Some fast type parent fibers are weakly or, more rarely, moderately immunopositive for embryonic isomyosin. This indicates that reactivation of myogenesis may also depend on the fiber type. The level of atrophy, destabilization of the differentiated myofiber phenotype, and degenerative changes of individual fibers in denervated muscle are very heterogeneous. The myogenic response of the first type is associated predominantly with fibers of average and higher than average levels of atrophy. Muscle cells that undergo a lesser degree of atrophy also form daughter fibers, although with a lower incidence. We did not find any correlation between the size of newly formed fibers and the level of atrophy of parent fibers. The topographical distribution of new myotubes both in the peripheral and central areas of the mid-belly equatorial sections at the early stages following nerve transection indicates that myogenesis of the first type represents a systemic reaction of muscle to the loss of neural control. These data indicate that activation of the myogenic response does not depend on cell death and degenerative processes per se. The second type of myogenesis is a typical regenerative reaction that occurs mainly within the spaces surrounded by the basal laminae of dead muscle fibers. Myocytes of different sizes are susceptible to degeneration and death, which indicates that cell death in denervated muscle does not correlate with levels of muscle cell atrophy. The regenerative process frequently results in development of abnormal muscle cells that branch or form small clusters. Replacement of lost fibers becomes activated between 2 and 4 months following nerve transection, i.e., mainly at advanced stages of postdenervation atrophy, when cell death becomes a contributing factor of the atrophic process. In long-term denervated muscle, the first and second types of myogenesisoccur concurrently, and the topographical distribution of the myogenic response becomes more heterogeneous than during the first weeks following denervation. Thus, our data demonstrate differential temporal and spatial expression of two patterns of myogenesis in denervated muscle that appear to be controlled by different regulatory mechanisms during the postdenervation period. (c) 2001 Wiley-Liss, Inc.

Animals↗
PubMed2004

FGF6 mediated expansion of a resident subset of cells with SP phenotype in the C2C12 myogenic line.

Fibroblast growth factor 6 (FGF6) is selectively expressed during muscle development and regeneration. We examined its effect on muscle precursor cells (mpc) by forcing stable FGF6 expression in C2C12 cells in vitro. FGF6 produced in genetically engineered mpc was active, inducing strong morphological changes, altering cell adhesion and compromising their ability to differentiate into myotubes. Expression of MyoD and myogenin, but not of Myf5, was abrogated in FGF6 engineered mpc. These effects were reversed by FGF inhibitors. Ectopic expression of MyoD also restored fiber formation indicating that FGF6 interferes with the myogenic differentiation pathway upstream of MyoD. We also report that in the presence of FGF6, the minor (0.5-2%) subpopulation of cells actively excluding Hoechst 33342 in a verapamil-dependent manner (SP phenotype) was increased to 15-20% and the expression of the mdr1a gene (but not mdr1b) was upregulated by 400-fold. Our data establish a previously undescribed link between FGF6--a muscle specific growth factor--and a multidrug resistance gene expressed in stem cells, and suggest a role for FGF6 in the maintenance of a reserve pool of progenitor cells in the skeletal muscle.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1991

Human ontogenesis. 3. Cell death in fetal muscle.

Naturally occurring muscle cell death in normal human fetal muscle was examined to determine the timing and structural differences with respect to muscle maturity. Two types of degenerative changes in developing muscle were found: cytoplasmic and nuclear. Degeneration of the primary and mature myotubes between 10 and 16 weeks of gestation entailed cytoplasmic condensation and disruption, swelling of mitochondria and dilatation of sarcoplasmic reticulum. In contrast, the formation of immature muscle fibres was associated with disintegration of satellite myofibres characterized by nuclear degenerative changes. These findings indicate that naturally occurring muscle cell death appears as a two-successive-stage phenomenon of cell necrosis. Initially, at the myotube stage, a number of muscle cells are eliminated. In the later stage a single cell is removed from the cluster which seemingly is responsible for final shape and size of the muscle fibre.

Cell Nucleus↗
PubMed2005

Congenital myopathy with arrest of myogenesis prior to formation of myotubes.

We report a novel type of congenital myopathy, which is characterized by an early arrest of muscle formation prior to formation of myotubes. A female infant born prematurely at 32 weeks of gestational age died after six weeks of continuous ventilatory support. Various muscle specimens including quadriceps, deltoid, pectoral, neck, psoas, tongue, and diaphragm musculature were studied. Light and electron microscopy revealed well-demarcated fascicular structures interspersed with undifferentiated, mononuclear myogenic cells. Multinucleated myotubes and muscle fibres were not detectable, pointing towards a defect prior to the generation of myotubes during myogenesis. Immunohistochemistry identified the absence of dystrophin, N-CAM, MyoD and myogenin expression in these myogenic cells, compatible with a block of the complex transcriptional network necessary for correct embryonic muscle formation at an early stage of muscle development. These myopathological findings were absent in cardiac muscle, indicating that the defect exclusively affects skeletal muscle formation.

Female↗
PubMed1986

Ultrastructure of developing human muscle: the problem of multinucleation of striated muscle cells.

The authors studied by electron microscopy the muscle of 27 human foetuses ranging from 9 weeks to 9 months development. It was possible to observe that disintegration of the plasma membranes of adjacent myoblasts and myotubes which share a common basement membrane tube appears to occur in longitudinally disposed cells of those categories. This may help to explain how further nuclei may be incorporated into well developed myotubes and how the striated muscle cells become multinucleated during embryonic myogenesis and regeneration in vivo.

Basement Membrane↗
PubMed2003

[Molecular cloning, expression mutation of myostatin and study on biochemical activity of its C-terminal peptide].

Myostatin, a member of the TGF-beta family, negatively regulates skeletal muscle development. Mutation of myostatin activity leads to increases muscle growth and carcass lean yield. The bovine myostatin mutation cDNA was amplified by polymerase chain reaction, and then sub-cloned into the expression vector pET-30a( + ) to form the expression plasmid pET30a (+)-action/ Myostatin. The recombinant plasmid was transformed into E. coli BL21. The overexpression product of pET30a (+)-action/ Myostatin was been showed in vitro. Sheep skeletal muscle cell were cultured with the purified myostatin mutation C-terminal peptide. The results of this study suggest that had a powerful activity to stimulate the hyperplasia and proliferation of sheep muscle cells and shows high biochemical activity.

Animals↗
PubMed1995

Both basic fibroblast growth factor and ciliary neurotrophic factor promote the retention of polyneuronal innervation of developing skeletal muscle fibers.

At birth, nearly all rat muscle fibers receive synaptic inputs from more than one motoneuron at a single end-plate site. By the end of the third postnatal week all but one of these inputs has been eliminated. During this loss of polyneuronal innervation, developing neuromuscular synapses compete with one another. Although the nature of this competition is not known, it is commonly assumed that it is mediated through differential activity of the competing inputs. One means by which such differential activity might be translated into a biological signal would be if the synapses compete in an activity-dependent manner for a scarce supply of neurotrophic molecules. A prediction of this hypothesis is that excess quantities of such trophic molecules will reduce competition and thereby slow down or abolish the normal loss of polyneuronal innervation. In newborn rats, the effects of injection of either basic fibroblast growth factor (bFGF) or ciliary neurotrophic factor (CNTF) on the outcome of neuromuscular synapse elimination were investigated. Daily injections of either bFGF or CNTF were made for 1 week into the lateral gastrocnemius muscle beginning at the postnatal age of 2 days. The amount of polyneuronal innervation of fibers in trophic molecule-injected muscles and saline-injected contralateral muscles was assayed using intracellular recording methods. For both bFGF- and CNTF-injected muscles, an increase in the percentage of polyneuronally innervated fibers relative to saline-injected muscles was noted. For bFGF-injected muscles, the amount of polyneuronal innervation remained at nearly 60% as late as the postnatal age of 14 days (P14). This is the amount of polyneuronal innervation found at age 6 days in normal animals. Nearly 40% of the fibers of CNTF-injected muscles remained polyneuronally innervated at age P14, the amount expected at age 9 days. These results indicate that both bFGF and CNTF exert powerful and long-lasting effects on developing neuromuscular synapses.

Animals↗
PubMed1978

Observations on the development of muscle hypersensitivity following chronic nerve conduction blockage and recovery.

Agar-sleeves containing 0.01%, 0.015% and 0.02% Tetrodotoxin were placed onto the sciatic nerve of the rat. The time-course of the conduction block and the full recovery of the nerve were studied; correlations were drawn with the hypersensitivity developed on the innervated muscles. The earliest sign of a TTX-produced conduction block was a decrease in the amplitude of the faster conducting fibres appearing 3 min later. Complete block was fully established 35 min later. The duration of a complete conduction block was a dose-dependent phenomenon and lasted from 1--4 days. The recovery process was gradual, simulating the reverse pattern of the acute TTX-block but spread over a much longer period with complete conduction recovery occuring 12 to 13 days later. Innervated muscles behaved as paralytic even before the complete establishment of a conduction block and remained so for 2--6 days after which clinical recovery was prompt. Muscles innervated by the TTX-treated nerves developed hypersensitivity to acetylcholine which could be seen within two days. This hypersensitivity continued to increase over the following days, despite some recovery of conduction. Its maximum appeared six to seven days later and then declined to return to normal at the time when nerve conduction properties had fully recovered. A similar degree of partial conduction block when acutely established always resulted in paralysis but when chronically present, the clinical picture of paralysis was fully compensated, due to the hypersensitivity of the muscle and possibly to collateral nerve sprouting.

Action Potentials↗
PubMed2003

IGF-II transcription in skeletal myogenesis is controlled by mTOR and nutrients.

Insulin-like growth factors (IGFs) are essential for skeletal muscle development, regeneration, and hypertrophy. Although autocrine actions of IGF-II are known to initiate myoblast differentiation, the regulatory elements and upstream signaling pathways for myogenic expression of IGF-II remain elusive. Here, we report the regulation of IGF-II transcription by mTOR, as well as by amino acid sufficiency, through the IGF-II promoter 3 and a downstream enhancer during C2C12 myoblast differentiation. Furthermore, we present evidence that IGF production, and not IGF signaling, is the primary target for mTOR's function in the initiation of differentiation. Moreover, myogenic signaling by mTOR is independent of its kinase activity and mediated by the PI3K-Akt pathway. Our findings represent the first identification of a signaling pathway that regulates IGF-II expression in myogenesis and implicate the mTOR-IGF axis as a molecular link between nutritional levels and skeletal muscle development.

Amino Acids↗
PubMed1994

Persistent expression of tissue-specific troponin T isoforms in transplanted chicken skeletal muscle.

This study attempted to investigate the expression of skeletal muscle troponin T isoforms in chicken reared for six months after muscle transplantations of breast muscle into leg muscle, leg muscle into breast muscle, and slow muscle into breast and leg muscles of the same animal. The regenerated muscle after transplantation was studied by histological observation, two-dimensional SDS-polyacrylamide gel electrophoresis, and immunoblotting with anti-troponin T antibodies. Persistent expression of troponin T isoforms specific to donor tissue was observed in the regenerated muscle, and compared with their expression in the normal developing muscles. During the regeneration, the cells grew up and expressed troponin T isoforms in a manner similar to that in normal developing muscles, and on around the 178th day after the transplantation, the regenerated muscle expressed the adult type troponin T isoforms. Based on the troponin T isoforms expressed in the transplants, we consider that one type of skeletal muscle has some inherent potential to grow in and coexist with other types for a long term.

Animals↗
PubMed1995

Effect of stunning amperage on broiler breast muscle rigor development and meat quality.

Two experiments were conducted to determine the effects of constant amperage (as opposed to constant voltage) electrical stunning on broiler blood loss, post-mortem breast muscle (Pectoralis major) rigor development, and breast meat quality. Broilers were individually stunned for 5 s at 0 (unstunned control group), 50, 100, 150, and 200 mA in Experiment 1 and at 0, 50, and 125 mA in Experiment 2. Breast muscle pH and R-value (ratio of adenosine to inosine nucleotides) were determined at 15 min and 24 h post-mortem; breast meat shear value and color were determined at 48 h post-mortem. Stunning amperage had no effect on percentage blood loss in either experiment. The most rapid post-mortem reactions were observed for the unstunned control group as determined by pH and R-value at 15 min post-mortem. Birds stunned with 50 mA were intermediate with regard to rate of rigor development. The slowest post-mortem reactions occurred in broilers stunned from 100 to 200 mA. There were no differences in pH, R-value, or color between stunning treatments after carcasses were aged for 24 h. Stunning amperage did not affect Allo-Kramer shear value for breast muscles deboned at 15 min post-mortem. In Experiment 2, 24 h aged breast meat from broilers stunned with 125 mA required significantly higher shear value (4.5 kg/g) than breast meat from broilers stunned at 0 or 50 mA (3.8 and 3.6 kg/g, respectively). Results indicate that stunning amperages between 0 and 200 mA had effects on the rate of early rigor development but there were no consistent effects on final breast meat quality.

Animals↗
PubMed1995

Immunolocalization of triadin, DHP receptors, and ryanodine receptors in adult and developing skeletal muscle of rats.

The dihydropyridine receptors (DHPR) and the ryanodine receptors (RyR) are well-characterized proteins of the triad junctions of skeletal muscle fibers. Recently, a newly discovered 95-kDa protein, triadin, has been purified from rabbit skeletal muscle heavy sarcoplasmic reticulum (SR) vesicles. WE have used indirect immunogold EM to localize triadin to the junctional face of the SR in isolated triads. In addition, we have used indirect immunofluorescence to localize triadin in relation to the DHPR and the RyR in adult and developing rat skeletal muscle. In double immunolabelling experiments of longitudinally oriented adult rat skeletal muscle tissue, triadin-specific and RyR-specific antibodies resulted in a characteristic striated staining pattern. The staining arising from these antibodies completely overlapped when examined by computer analysis of digitized laser scanning confocal microscopy images. A similar result was obtained in double staining experiments using antibodies raised against the DHPR and the RyR suggesting that all three proteins are located in the triads in situ. The developmental expression of the three triad proteins was examined using double labeling of skeletal muscle tissue from several fetal and early postnatal ages. The staining patterns of triadin, RyR, and DHPR antibodies were overlapping throughout development, suggesting that from their earliest appearance the three proteins are components of the triads.

Aging↗
PubMed1992

A method to assess the development of muscle power in preterms after term age.

The purpose of this paper is to report a detailed description of an instrument for evaluating the development of active and passive muscle power in preterms beyond term age. The instrument is constructed on a basis of age-specific items that assess these two components of muscle power and on the assumption that a persistent discrepancy between them serves to detect those preterms at most risk for disturbances in motor development. The application of the instrument is illustrated by reporting the individual trajectories of five case studies without any serious medical complications. It is concluded that if a marked discrepancy between active and passive power persists beyond the corrected age of 3 months, then this may be a sign of underlying pathology which will eventuate in abnormal postural outcomes and thereby disturbances in the control and coordination of movement. Having now provided a detailed description of how this instrument should be applied in postterm follow-up of preterm infants, we are currently examining its sensitivity and specificity on a much larger sample of similar subjects.

Age Factors↗
PubMed2004

The novel mouse connexin39 gene is expressed in developing striated muscle fibers.

The recently identified mouse connexin39 (mCx39) gene encodes a peptide of 364 amino acids that shows only 61% sequence similarity to its putative human orthologue connexin40.1 (hCx40.1). The coding regions of mCx39 and hCx40.1 are located on two different exons as described for murine and human connexin36. Northern blot and RT-PCR analyses revealed that mCx39 is expressed after embryonic day (ED) 13.5 up to birth and is absent from the adult stage. Polyclonal antibodies raised to a peptide corresponding to the 16 C-terminal amino acid residues detected a protein band of about 40 kDa apparent molecular mass in lysates of several embryonic tissues. In sections of ED14.5, ED16.5 and neonatal (P0) tissues, immunofluorescent signals were prominent between myotubes in the developing diaphragm, within the intercostal muscle, in the region around the occipital bone, as well as in muscles of the limb, tongue and connective tissue around the eye. These antibodies yielded punctate signals on apposed plasma membranes of HeLa cells transfected with Cx39 cDNA but did not react with wild-type cells. Furthermore, no intercellular permeation of microinjected neurobiotin and other tracers could be detected in Cx39 transfected HeLa cells. However, after microinjection of Alexa488 into myotubes of dissected neonatal diaphragm, we found spreading of this dye into neighbouring cells. As expression of no other known connexin could be verified in these cells, intercellular dye transfer might result from functional expression of Cx39 in developing striated muscle fibers.

Amino Acid Sequence↗
PubMed1987

Calcium channel components of action potential in chick skeletal muscle cells developing in culture.

The action potential was recorded from cultured chick skeletal muscle cells in Na-, Ca-, Cl-free saline containing Ba and tetraethylammonium ions (Ba saline). The action potential consisted of two components: a low-threshold, fast inactivating component and a high-threshold, long-lasting component. Both components of the action potential were dependent on external Ba ions and eliminated by Co ions. It is concluded that both components are generated by inward currents carried by Ba ions through Ca channels. The two Ca channel components of the action potential differed with regard to activation and inactivation potential, presence or absence of fast inactivation, sensitivity to an organic Ca channel blocker, and developmental profile. In addition, the failure of occurrence of one or the other components was observed in some cells. These results could be explained by assuming that two components of the action potential in Ba saline were mediated by the two different Ca channels. Furthermore, there was a tendency for younger cells to have more prominent Ca channel components. This may suggest that Ca channels have some function in the early stages of myogenesis.

Action Potentials↗